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Up to 15% of patients with chronic spontaneous urticaria (CSU) experience severe exacerbations of their baseline cutaneous disease after taking nonsteroidal anti-inflammatory drugs that inhibit cycloxygenase-1 (COX-1) enzyme. These subjects are defined as having a NECD (NSAID-exacerbated cutaneous disease). The way NSAID hypersensitivity correlates with the different pathogenic mechanisms of CSU has not been investigated so far. 235 adults with severe CSU submitted to omalizumab treatment were studied. A rapid omalizumab response was considered as a marker of auto-allergic (Type I) CSU whereas patients showing a slow response or not responding at all were regarded as having a type IIb autoimmune disease. At the first visit medical history of tolerance to aspirin and/or other COX-1 inhibiting NSAID was ascertained. Duration of disease, atopic status, thyroid autoimmunity, CRP, D-dimer plasma levels, and total IgE were assessed appropriately. 23 (10%) were hypersensitive to NSAID. Patients with or without did not differ in any of the variable considered, and a similar proportion in the two groups showed type I or type IIb CSU. The study suggests that in CSU hypersensitivity to NSAID represents a phenomenon that is independent on the pathogenesis of the underlying skin disease.

Nonsteroidal anti-inflammatory drugs hypersensitivity in chronic spontaneous urticaria in the light of its pathogenesis